This Is MS Multiple Sclerosis Community: Knowledge & Support

Welcome to the world's leading forum on Multiple Sclerosis research, support, and knowledge. For over 10 years, This is MS has provided an unbiased community dedicated to Multiple Sclerosis patients, caregivers, and affected loved ones.

Bethr wrote:Zeureka, that's exactly what happened to me, I had my one and only lesion when my Transferrin Saturation was high, well actually the month after the blood test I got to see why I was so fatigued and sleepy.I don't recognise the word Sideremia, is that ferritin? If it is, mine was never above 175, yet I am iron overloaded.

Department of Biology and Medical Genetics, School of Medicine, University of Rijeka, Braće Branchetta 20, 51000 Rijeka, Croatia. smiljana.ristic@mamed.medri.hr

In the present study we have investigated whether HFE gene polymorphism may play a role in the disease process of Croatian and Slovenian MS patients and their potential genetic susceptibility to MS. We genotyped 314 MS patients and 400 healthy controls for the C282Y and H63D mutations by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP) analysis. Our results showed no significant differences in the distribution of the two mutations between MS patients and controls, suggesting that HFE polymorphisms do not contribute to the susceptibility to MS. Also, there was no significant correlation between HFE polymorphism and the disease progression index. However, we observed that MS patients carrying the mutant C282Y allele exhibited earlier onset of disease symptom relative to other genotypes, but it warrants further study in a larger series of MS patients.

I'm sure it's not that simple . Maybe I have some other problem that makes it stand out on me. I have appointments with the hemotologist and the nuerologist coming up soon, they may shed some light on it. For some reason it was really obvious to me as whenever I had blood loss I felt much better, and didn't sleep on those days, the bigger the loss the better I felt.
I can't seem to find any pics of the pigmentation on arms, but the women at this link has it on her face. Mine is similar, a patchy tan, with a slightly different colour than your usual tan, it has a slight grey tinge to it.
My brother has it on his forearms, so do I.

zinc deficiency and hyperpigmentation are known to be connected. as well as zinc and iron regulation.

found an abstract on zinc deficiency and three kinds of cutaneous signs in adults, including hyperpigmentation - anyone here speak hungarian and have full access to this journal??

Orv Hetil. 2004 May 9;145(19):1007-10.
[Cutaneous symptoms of zinc deficiency in adults]
[Article in Hungarian]
Malabsorption is frequently accompanied by skin symptoms, which are the most likely first manifestation of the disease. Skin lesions are mainly due to the deficiency of zinc, different vitamins, minerals, essential aminoacids, and other nutrients. The present paper demonstrates 3 patients with different types of skin symptoms primarily related to zinc deficiency, which occur in gastrointestinal diseases and alcohol abuse (acrodermatitis enteropathica, eczema craquele, hyperpigmentation).

melasma (pregnancy mask) could be connected to zinc also. pregnancy is a big zinc drain for moms.

bethr i must have already asked you if you know your zinc level, or are planning on having it looked at?

I'll ask about it Jimmylegs, when I get to the specialists.
I don't take pills or vitamins at all, never have. No prescribed drugs, painkillers, nothing. I'd rather keep myself ala naturelle, until I get tested.

hi b, yea i felt that way too until ms taught me i was doing it wrong.. when i finally did tests the levels were bad.. i still played games.. until i really crashed then i started getting serious with testing.. multiple deficiencies.. tried low level supplements and realized how ineffective they can be.. have spent 4 years learning the intricacies... lots more to learn in future!

Hi Jimmy, I now know that I have PCT (porphyria Cutanea Tarda) in a deadly combination with iron loading Hemochromatosis (I have one gene C282Y). I will load iron whilst being in the acceptable range, so no doctor will pick up on it.

We'll see soon, but I should have elevated zinc levels.

PCT can give you lesions and some symptoms similar to MS.
The iron overload makes you fatigued and stiffens your joints.
It comes in "attacks" similar to MS.
I don't have MS, neither does my sister who was diagnosed with MS 20 years ago.

Both PCT and hemochromatosis are treated by phlebotomy, diet and careful monitoring, with phlebs as needed.
The outlook is great so long as you know you have it!

hey there, that is great that you have figured out what you're dealing with! i dug up some abstracts on PCT and possibly relevant/related stuff:

Ascorbic acid deficiency in porphyria cutanea tarda1Journal of Laboratory and Clinical Medicine, Volume 130, Issue 2, Pages 197-201Porphyria cutanea tarda (PCT), the most common form of porphyria, is manifested as skin photosensitivity caused by excess hepatic production of uroporphyrin and heptacarboxylporphyrin. In experimental animal models, ascorbic acid modulates chemically induced uroporphyrin accumulation. The purpose of this study was to determine whether ascorbic acid is decreased in the plasma of patients with PCT. Plasma was obtained after an overnight fast from 21 PCT patients, 16 of whom were infected with hepatitis C virus (HCV), and from a separate group of 9 patients with HCV infection but not PCT. Thirteen PCT patients were studied when they had active disease and 8 after treatment-induced Plasma ascorbic acid was low (<23 μmmol/L) in 11 (85%) of the 13 untreated PCT patients and deficient (<11 μmol/L) in 8 (62%). Two patients with normal ascorbic acid levels (45 and 62 μmol/L) had consumed multivitamins. In 2 patients with deficient ascorbic acid, plasma levels returned to normal after phlebotomy treatment. Of the 8 patients studied during remission, 4 had normal ascorbic acid values and 4 were deficient (5 to 8 μmol/L). Plasma ascorbic acid values were normal for all patients who had HCV but no PCT. These data suggest that plasma ascorbic acid concentrations are commonly low in PCT, but this decrease is unrelated to HCV infection. Ascorbic acid deficiency may be one of the factors that contributes to the pathogenesis of PCT.

so i wonder about that deficiency/causal notion .. maybe it's just that the high iron in your system causes a drain on ascorbic acid in the body? i think that could be more likely seeing that phlebotomy helps normalize the serum ascorbic acid without any supplements.

Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and wilson's diseaseJournal of Hepatology, Volume 20, Issue 1, Pages 41-46AbstractThe RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n=17; group A), hemochromatosis (n=17; group B) and Wilson's disease (n=12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (>180 μg/dl), a low free iron binding capacity (<8 μmol/l) and high ferritin-levels (<450 μg/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (>10 μg/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.

Supplemental therapy in isolated vitamin E deficiency improves the peripheral neuropathy and prevents the progression of ataxiaJournal of the Neurological Sciences, Volume 156, Issue 2, Pages 177-179AbstractA 24-year-old male, who suffered since childhood from a progressive form of ataxia associated with peripheral neuropathy, was found severely deficient in serum vitamin E. He walked with bilateral aid and presented severe dysmetria of the limbs and dysarthric speech; muscular strength and trophism were slightly diminished in the distal muscles of four limbs and there was hypotonia of the arms; he presented absent deep tendon reflexes, bilateral Babinski's sign, reduced proprioception at four limbs, pes cavus and fasciculations of the tongue. Intestinal fat malabsorption and other gastrointestinal or haematological conditions associated with deficiency of this vitamin were ruled out. In this patient, after 2 years of a daily supplement of high doses of vitamin E, a further progression of the disease was not observed and, moreover, the neurophysiological characteristics of his neuropathy appeared clearly improved. A longitudinal evaluation of serum vitamin E levels showed values in the normal range after 13 months of therapy. The patient had molecular genetic analysis of chromosome 8 and was found homozygous for the unusual mutation 513insTT in the α-tocopherol transfer protein gene.

Quad Sclavo Diagn. 1982 Sep;18(3):249-57.[Zinc and porphyria cutanea tarda][Article in Italian]In 30 patients affected by Porphyria Cutanea Tarda we determined: plasmatic, erythrocytary and urinary zinc (by atomic absorption spectrophotometry); total porphyrins in plasma and in urines, coproporphyrins and protoporphyrins in erythrocytes (by spectrophotometric methods); haptoglobin, hemopexin, alpha 2-macroglobulin and albumin (by immunological methods). The results obtained were compared with those of normal subjects. In addition, the variables under consideration were statistically analyzed to bring out possible correlations (both simple and partial). The most interesting result (besides the documentation of an increase in the urinary and plasmatic zinc in porphyric patients) was the finding of correlations between plasmatic zinc, plasmatic porphyrins and alpha 2-macroglobulin.

delta-Aminolaevulinate dehydratase activity was measured in liver biopsy specimens from 13 patients with porphyria cutanea tarda, 13 alcoholics and 10 control subjects. The mean enzyme activities in liver of porphyria cutanea tarda and alcoholics were 34% (P less than 0.001) and 49% (P less than 0.001) respectively of the control level. Heat treatment of liver supernatant caused slight inhibition of the enzyme activity in porphyria cutanea tarda and in controls. Addition of Zn2+ to liver supernatants slightly increased the enzyme activity in both porphyria cutanea tarda and controls. The addition of liver supernatant from the porphyria cutanea tarda to purified bovine delta-aminolaevulinate dehydratase did not result in suppression of the enzyme activity. The apparent Km value of delta-aminolaevulinate dehydratase was 4.3 X 10(-4) mol/l for porphyria cutanea tarda livers and 3.3 X 10(-4) mol/l for control livers. The difference between the two was not significant.

The erythrocyte delta-aminolevulinic acid dehydratase activity was studied in porphyria cutanea tarda patients, compared to healthy controls, in an attempt to resolve the contradictions in the relevant literature data. In an in vitro experimental system, a study was also made of how the erythrocyte delta-aminolevulinic acid dehydratase activity varies on the action of the activators -SH and Zn2+. It was found that, compared to the healthy controls, the erythrocyte delta-aminolevulinic acid dehydratase activity of porphyria cutanea tarda patients is significantly decreased, but it is restored to the original activity level on the addition of -SH and Zn2+. Since there is a general -SH requirement of delta-aminolevulinic acid dehydratase, the most obvious explanation for the decrease of the activity in the case of the patients is the shift of the natural redox systems of the erythrocytes, and the decrease of the reduced glutathione/oxidized glutathione ratio

Background: Copper deficiency in ruminants is known to cause an ataxic myelopathy. Copper deficiency as a cause of progressive myelopathy in adults is underrecognized.

Objective: To describe the clinical, biochemical, electrophysiologic, and imaging characteristics in 13 patients with myelopathy associated with copper deficiency.

Methods: The records of patients with a copper deficiency–associated myelopathy were reviewed. Clinical characteristics, laboratory investigations, and responses to therapeutic intervention were summarized.

Results: Thirteen such patients were found, 11 of them in a 15-month period. All patients presented with prominent gait difficulty, reflecting a sensory ataxia due to dorsal column dysfunction and lower limb spasticity. All patients had polyneuropathy. A high or high-normal serum zinc level was seen in 7 of the 11 patients for whom this information was available. Somatosensory evoked potential studies done in eight patients showed impaired conduction in central proprioceptive pathways. Dorsal column signal change on spine MRI was present in three patients. An initial clue to the diagnosis was a very low ceruloplasmin level; further tests of copper metabolism excluded Wilson disease. The cause remained unexplained in most patients. Oral copper supplementation restored normal or near-normal copper levels in 7 of the 12 patients in whom adequate follow-up data were available; parenteral supplementation restored normal level in 3 further patients. Copper supplementation prevented further neurologic deterioration, but the degree of actual improvement was variable.

Conclusions: Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults. The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency. Early recognition and copper supplementation may prevent neurologic deterioration.

i can't find out why the zinc would be elevated.. i'm curious if it's somewhat similar to the hypercalcemia seen in excess vit d3.. but anyway, just a bunch of stuff to read

I thought I'd drag this one out again, as I now have another tie-in.
I've done phlebotomy to reduce my iron levels, which are quite good now, and I'm feeling progressively better with each big blood draw, blood test and with menstruation.

On my latest CBC blood test it has shown up Polycythemia, which is of course what happens to blood at altitude, it thickens, too many red blood cells. I don't live at altitude!

The main trestment for Polycythemia is phlebotomy!
So I may be suffering some type of hypoxia? Genetic/acquired?

I'm up for further blood tests in a few weeks, and it will be very interesting to see the tie in.

My Wife Girlfreind Had a brain meltdown on the way from San jose UsAirways after her 2nd stent,which was to be a checkup,This Dr,Dake @@@@@@ -Guinea Pig Surgery,How Vascular Surgeons and Neu Docs are conecected is beyond me.Go for it Dr.Dake ,Let the Blood flow.

Who is online

This site does not offer, or claim to offer, medical, legal, or professional advice.
All treatment decisions should always be made with the full knowledge of your physicians.
This is MS does not create, endorse, or republish any content.
All postings are the responsibility of the poster. All logos and trademarks in this site are property of their respective owners. All users must respect our rules for intellectual property rights.